Medical Physiology Pp2 Year 2

Good Luck Daktari #### **SECTION A: SHORT ANSWER QUESTIONS (Total – 60 Marks)** **Each question carries 5 marks. All questions are compulsory.** - **Gastrin** is a peptide hormone secreted by **G cells** in the antrum of the stomach. - Stimulated by **peptides/amino acids, stomach distension, and vagal stimulation (via GRP)**. - **Increases gastric motility** by enhancing **contractions of the gastric smooth muscle**. - **Promotes gastric emptying** by increasing the tone of the **lower esophageal sphincter**, relaxing the **pyloric sphincter**, and stimulating **antral contractions**. - Indirectly stimulates **motility of the small intestine** via increased gastrin-mediated secretions. - Enhances **peristaltic movements**, thus aiding in mixing and propulsion of gastric contents. - Excess gastrin (e.g., in **Zollinger-Ellison syndrome**) can lead to **hyper-motility and diarrhea**. **Inhibition of Pancreatic Autodigestion** - Pancreatic enzymes are synthesized and secreted as **inactive zymogens** (e.g., trypsinogen). - **Trypsinogen** is activated only in the **duodenum** by **enterokinase (enteropeptidase)**. - The pancreas also secretes **trypsin inhibitor** (e.g., **SPINK1**) to prevent premature trypsin activation. - **Compartmentalization** of enzymes in **zymogen granules** within acinar cells prevents cytoplasmic exposure. - The **ductal cells** secrete **bicarbonate**, flushing enzymes into the duodenum and diluting them. - Any prematurely activated trypsin is rapidly inactivated by **autolysis or inhibitors**. - Disruption of these safety mechanisms (e.g., in pancreatitis) leads to **autodigestion**. **Process of Digestion of Fats** - Begins in the **mouth (lingual lipase)** and **stomach (gastric lipase)** – minor role. - Major digestion occurs in the **small intestine**, especially **duodenum and jejunum**. - **Emulsification** by **bile salts** increases surface area for enzyme action. - **Pancreatic lipase** (with **colipase**) hydrolyzes triglycerides into **monoglycerides and free fatty acids**. - These products form **micelles** with bile salts for transport to the **intestinal brush border**. - Absorbed into **enterocytes**, where triglycerides are **re-esterified**. - Packaged into **chylomicrons** and transported via **lacteals into lymphatics**. **Physiology Behind Satiety After a Heavy Meal** - **Stomach distension** activates **mechanoreceptors** that signal the **hypothalamus (satiety center)** via **vagal afferents**. - **Cholecystokinin (CCK)** is released from the **duodenum** in response to fats and proteins, slowing gastric emptying and promoting satiety. - **Insulin and GLP-1** rise postprandially and act on the **arcuate nucleus** of the hypothalamus to inhibit hunger. - **Leptin** (from adipose tissue) exerts longer-term satiety effects but contributes postprandially. - **PYY** from the ileum/colon also contributes to **delayed gastric emptying and reduced appetite**. - **Serotonin** (from enterochromaffin cells) contributes to early satiety by modulating enteric and central pathways. - Integration of **neural and hormonal signals** leads to inhibition of the **lateral hypothalamic (hunger) center** and activation of the **ventromedial nucleus (satiety center)**. **Effects of Thyroid Hormones on the Cardiovascular System** - **Increased heart rate (positive chronotropic effect)**: Thyroid hormones enhance the sensitivity of the heart to catecholamines, increasing heart rate. - **Increased cardiac output**: Both heart rate and stroke volume are elevated, leading to an increase in cardiac output. - **Increased myocardial contractility (positive inotropic effect)**: Thyroid hormones increase the force of myocardial contraction. - **Peripheral vasodilation**: Thyroid hormones cause vasodilation in peripheral vessels, lowering systemic vascular resistance. - **Increased blood volume**: Thyroid hormones increase sodium and water retention by the kidneys, contributing to increased blood volume. - **Arrhythmias**: Hyperthyroidism can lead to arrhythmias, including atrial fibrillation, due to increased myocardial excitability. - **Enhanced oxygen consumption**: Increased metabolic rate from thyroid hormones raises myocardial oxygen demand. **Physiological Functions of the Pancreatic Hormone Glucagon** - **Increases blood glucose levels**: Glucagon stimulates **glycogenolysis** in the liver, converting stored glycogen to glucose. - **Promotes gluconeogenesis**: Stimulates the liver to produce glucose from non-carbohydrate precursors (e.g., amino acids). - **Stimulates lipolysis**: Glucagon activates the breakdown of stored triglycerides into free fatty acids and glycerol. - **Increases ketogenesis**: In periods of fasting, glucagon stimulates the liver to convert fatty acids to ketone bodies. - **Inhibits insulin secretion**: Glucagon reduces insulin secretion to prevent hypoglycemia during fasting. - **Enhances protein catabolism**: Glucagon increases the breakdown of protei